Cardiovascular Journal of Africa: Vol 25 No 5 (September/October 2014)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 5, September/October 2014 AFRICA 243
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New culprit identified in metabolic syndrome
A new study suggests uric acid may play a role in causing the
metabolic syndrome, a cluster of risk factors that increases
the risk of heart disease and type 2 diabetes.
Uric acid is a normal waste product that is removed from
the body by the kidneys and intestines and is released in the
urine and stools. Elevated levels of uric acid are known to
cause gout, an accumulation of the acid in the joints. High
levels are also associated with markers of the metabolic
syndrome, which is characterised by obesity, high blood
pressure, and elevated blood sugar and cholesterol levels.
But it has been unclear whether uric acid itself is causing the
damage or it is simply a by-product of other processes that
lead to the dysfunctional metabolism.
New research from the Washington University suggests
that excess uric acid in the blood is no innocent bystander.
Rather, it appears to be a culprit in disrupting normal
metabolism. The research team states that uric acid may play
a direct, causative role in the development of the metabolic
syndrome. The work showed that the gut is an important
clearance mechanism for uric acid, opening the door to new
potential therapies for preventing or treating type 2 diabetes
and the metabolic syndrome.
Recent research by the senior author, Kelle H Moley, the
James P Crane professor of obstetrics and gynecology, and
her collaborators has shown that a protein called GLUT9 is
an important transporter of uric acid. The team studied mice
to learn what happens when GLUT9 stops working in the
gut, essentially blocking the body’s ability to remove uric acid
from the intestine. In this study, the kidney’s ability to remove
uric acid remained normal.
Eating regularly, mice missing GLUT9 only in the gut
quickly developed elevated uric acid in the blood and urine
compared with control mice. And at only six to eight weeks of
age, they developed the hallmarks of the metabolic syndrome:
high blood pressure, elevated cholesterol and blood insulin
levels, and fatty liver deposits, among other symptoms.
The researchers also found that the drug allopurinol,
which reduces uric acid production in the body and has
long been used to treat gout, improved some but not all of
the measures of metabolic health. Treatment with the drug
lowered blood pressure and total cholesterol levels.
Exposure to uric acid is impossible to avoid because it is
a normal byproduct of cell turnover in the body. But there is
evidence that diet may contribute to uric acid levels. Many
foods contain compounds called purines that break down
into uric acid. Adding to growing concerns about fructose
in the diet, evidence suggests that fructose metabolism in the
liver also drives uric acid production.
Switching to foods heavy-laden with fructose over the past
30 years has been devastating, according to Moley. ‘There’s a
growing feeling that uric acid is a cause, not a consequence, of
the metabolic syndrome. The medical community now knows
that fructose directly makes uric acid in the liver. With that in
mind, the laboratory is doing further research to study what
happens to these mice on a high-fructose diet.’
Source
1.
metabolic-syndrome
2. DeBosch BJ, Kluth O, Fujiwara H, Schurmann A, Moley KH.
Early-onset metabolic syndrome in mice lacking the intestinal uric
acid transporter SLC2A9. Nature Commun Aug 7, 2014.